Populations of fishes provide valuable services for billions of people, but face diverse and interacting threats that jeopardize their sustainability. Human population growth and intensifying resource use for food, water, energy and goods are compromising fish populations through a variety of mechanisms, including overfishing, habitat degradation and declines in water quality. The important challenges raised by these issues have been recognized and have led to considerable advances over past decades in managing and mitigating threats to fishes worldwide. In this review, we identify the major threats faced by fish populations alongside recent advances that are helping to address these issues. There are very significant efforts worldwide directed towards ensuring a sustainable future for the world's fishes and fisheries and those who rely on them. Although considerable challenges remain, by drawing attention to successful mitigation of threats to fish and fisheries we hope to provide the encouragement and direction that will allow these challenges to be overcome in the future.
Global environmental change is increasing hypoxia in aquatic ecosystems. During hypoxic events, bacterial respiration causes an increase in carbon dioxide (CO2) while oxygen (O2) declines. This is rarely accounted for when assessing hypoxia tolerances of aquatic organisms. We investigated the impact of environmentally realistic increases in CO2 on responses to hypoxia in European sea bass (Dicentrarchus labrax). We conducted a critical oxygen (O2crit) test, a common measure of hypoxia tolerance, using two treatments in which O2 levels were reduced with constant ambient CO2 levels (~530 µatm), or with reciprocal increases in CO2 (rising to ~2,500 µatm). We also assessed blood acid-base chemistry and haemoglobin-O2 binding affinity of sea bass in hypoxic conditions with ambient (~650 μatm) or raised CO2 (~1770 μatm) levels. Sea bass exhibited greater hypoxia tolerance (~20% reduced O2crit), associated with increased haemoglobin-O2 affinity (~32% fall in P50) of red blood cells, when exposed to reciprocal changes in O2 and CO2. This indicates that rising CO2 which accompanies environmental hypoxia facilitates increased O2 uptake by the blood in low O2 conditions, enhancing hypoxia tolerance. We recommend that when impacts of hypoxia on aquatic organisms are assessed, due consideration is given to associated environmental increases in CO2.
Fish in coastal ecosystems can be exposed to acute variations in CO2 of between 0.2-1 kPa CO2 (2,000 - 10,000 µatm). Coping with this environmental challenge will depend on the ability to rapidly compensate the internal acid-base disturbance caused by sudden exposure to high environmental CO2 (blood and tissue acidosis); however, studies about the speed of acid-base regulatory responses in marine fish are scarce. We observed that upon sudden exposure to ∼1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ∼40 minutes, thus restoring haemoglobin-O2 affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ∼2 hours, which is one of the fastest acid-base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3− in blood, which increased from ∼4 to ∼22 mM. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+ exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid-base regulation was completely prevented when the same high CO2 exposure occurred in seawater with experimentally reduced HCO3− and pH, likely because reduced environmental pH inhibited gill H+ excretion via NHE3. The rapid and robust acid-base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2 fluctuations that naturally occur in coastal environments.
Climate change causes warming, decreased O2, and increased CO2 in marine systems and responses of organisms will depend on interactive effects between these factors. We provide the first experimental assessment of the interactive effects of warming (14 to 22°C), reduced O2 (~3 – 21 kPa O2), and increased CO2 (~400 or ~1000 μatm ambient CO2) on four indicators of aerobic performance (standard metabolic rate, SMR, maximum metabolic rate, MMR, aerobic scope, and hypoxia tolerance, O2crit), blood chemistry, and O2 transport (P50) of a marine fish, the European sea bass (Dicentrarchus labrax). Warming increased SMR and O2crit (i.e. reduced hypoxia tolerance) as well as MMR in normoxia but there was an interactive effect with O2 so that hypoxia caused larger reductions in MMR and aerobic scope at higher temperatures. Increasing CO2 had minimal effects on SMR, MMR and O2crit and did not show interactive effects with temperature or O2 for any measured variables. Aerobic performance was not linked to changes in blood chemistry or P50. Despite lack of effects of CO2 on aerobic performance, increased CO2 induced 30% mortality of fish exercised in low O2 at 22°C indicating important threshold effects independent of aerobic performance. Overall, our results show temperature and O2, but not CO2, interact to affect aerobic performance of sea bass, disagreeing with predictions of the oxygen- and capacity-limited thermal tolerance hypothesis.
Predatory fish in the wild consume whole prey including hard skeletal parts like shell and bone. Shell and bone are made up of the buffering minerals calcium carbonate (CaCO3) and calcium phosphate (Ca3(PO4)2). These minerals resist changes in pH, meaning they could have physiological consequences for gastric acidity, digestion and metabolism in fish. Using isocaloric diets supplemented with either CaCO3, Ca3(PO4)2 or CaCl2 as non-buffering control, we investigated the impacts of dietary buffering on the energetic cost of digestion (i.e. specific dynamic action or SDA), gastric pH, the postprandial blood alkalosis (the “alkaline tide”) and growth in juvenile rainbow trout (Oncorhynchus mykiss). Increases in dietary buffering were significantly associated with increased stomach chyme pH, postprandial blood HCO3−, net base excretion, the total SDA and peak SDA but did not influence growth efficiency in a 21 day trial. This result shows that aspects of a meal that have no nutritional value can influence the physiological and energetic costs associated with digestion in fish, but that a reduction in the SDA will not always lead to improvements in growth efficiency. We discuss the broader implications of these findings for the gastrointestinal physiology of fishes, trade-offs in prey choice in the wild, anthropogenic warming and feed formulation in aquaculture.
The hypoxic constraint on peak oxygen uptake (ṀO2peak) was characterized in rainbow trout over a range of ambient oxygen tensions with different testing protocols and statistical models. The best-fit model was selected using both statistical criteria (R2 & AIC) and the model's prediction of three anchor points for hypoxic performance: critical PO2 (Pcrit), maximum ṀO2 and a new metric, the minimum PO2 that supports 50% of absolute aerobic scope (PAAS-50). The best-fitting model was curvilinear using five strategically selected PO2 values. This model predicted PAAS-50 as 70 mm Hg (CV=9%) for rainbow trout. Thus, while a five-point hypoxic performance curve can characterize the limiting effects of hypoxia in fish, as envisioned by Fry over 75 years ago, PAAS-50 is a promising metric to compare hypoxic constraints on performance in a standardized manner both within and across fish species.
Fish in coastal ecosystems can be exposed to acute variations in CO2that can approach 1 kPa CO2(10,000 μatm). Coping with this environmental challenge will depend on the ability to rapidly compensate the internal acid-base disturbance caused by sudden exposure to high environmental CO2(blood and tissue acidosis); however, studies about the speed of acid-base regulatory responses in marine fish are scarce. We observed that upon exposure to ~1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ~40 minutes, thus restoring haemoglobin-O2affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ~2 hours, which is one of the fastest acid-base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3− in blood, which increased from ~4 to ~22 mM. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid-base regulation was completely prevented when the same high CO2exposure occurred in seawater with experimentally reduced HCO3− and pH, likely because reduced environmental pH inhibited gill H+excretion via NHE3. The rapid and robust acid-base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2fluctuations that naturally occur in coastal environments.Summary statementEuropean sea bass exposed to 1 kPa (10,000 μatm) CO2regulate blood and red cell pH within 2 hours and 40 minutes, respectively, protecting O2transport capacity, via enhanced gill acid excretion.
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